LDL and apoB
CETP activity, not LDL receptor pathways, may explain why LDL cholesterol rises with dietary fat in some people (Curr Opin Lipidol 1997)
Original title: Response of low density lipoprotein cholesterol levels to dietary change: contributions of different mechanisms
This brief review addresses why LDL-cholesterol rises in some individuals following increased dietary cholesterol or saturated and trans-monounsaturated fatty acid intake, while in others a compensatory reduction in cholesterogenesis fully offsets these effects. In dietary responders, the review proposes that much of the observed LDL-cholesterol increase results directly from a rise in plasma CETP activity, through a mechanism that is not mediated by hepatic LDL receptors. This distinguishes CETP-driven LDL elevation from the classical LDL receptor-dependent pathway typically invoked to explain dietary cholesterol responsiveness.
Original abstract
In many individuals, LDL-cholesterol levels rise following increased consumption of dietary cholesterol or saturated and trans-monounsaturated fatty acids. In others, a reduction of cholesterogenesis fully compensates for these effects. In responding individuals, much of the increase in LDL-cholesterol observed may result directly from an increase in plasma cholesteryl ester transfer protein activity whose effect is not mediated by hepatic LDL receptors.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.